Abstract
The human immunodeficiency virus type 1 (HIV-1) capsid and its disassembly, or capsid uncoating, has remained an active area of study over the past several decades. Our understanding of the HIV-1 capsid as solely a protective shell has since shifted with discoveries linking it to other complex replication events. The interplay of the HIV-1 capsid with reverse transcription, nuclear import, and integration has led to an expansion of knowledge of capsid functionality. Coincident with advances in microscopy, cell, and biochemistry assays, several models of capsid disassembly have been proposed, in which it occurs in either the cytoplasmic, nuclear envelope, or nuclear regions of the cell. Here, we discuss how the understanding of the HIV-1 capsid has evolved and the key methods that made these discoveries possible.
Highlights
Human immunodeficiency virus type 1 (HIV-1) is a lentivirus in the retrovirus family that causes chronic infection, leading to the gradual depletion of CD4+ T cells and acquired immunodeficiency syndrome (AIDS) if untreated
As the HIV-1 capsid had been thought to be excluded from the nucleus, with uncoating preceding nuclear import, low levels of CA in the nucleus were viewed as residual protein remaining with the pre-integration complex (PIC) [78,86]
Decades of advancement in the tools available to detect CA, measure uncoating, quantify capsid stability, and determine interactions with host factors have increased the understanding of the HIV-1 capsid dramatically
Summary
Human immunodeficiency virus type 1 (HIV-1) is a lentivirus in the retrovirus family that causes chronic infection, leading to the gradual depletion of CD4+ T cells and acquired immunodeficiency syndrome (AIDS) if untreated. Antiretroviral therapy (ART) has advanced greatly, improving morbidity and mortality outcomes. As such, advancing our understanding of HIV-1 replication should continue, with the goal of developing novel therapeutics. The hallmarks of retroviral infection are reverse transcription of the viral single-stranded RNA (ssRNA) genome into double-stranded. HIV-1 does not require mitosis to access the chromatin, allowing the infection of nondividing cells. Post-entry HIV-1 replication events through integration remain a primary focus for antiretroviral development, with research often centered on understanding these processes. Biochemical, and microscopic techniques, our understanding of early HIV-1 replication has vastly improved
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